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Biomedical subjects

Z Zeng

Publications and source records attributed to Z Zeng.

At least 73 records · Page 4Linked to original sources
PubMed1999

Bone marrow pre-B-1 (Bomb1): a quantitative trait locus inducing bone marrow pre-B-cell expansion in lymphoma-prone SL/Kh mice.

Abnormalities of regulatory genes in early B-cell development often lead to lymphomagenesis. Our previous study showed that there is an abnormal transient expansion of bone marrow (BM) pre-B cells in lymphoma-prone SL/Kh strain mice. Such expansion is a genetic property of SL/Kh stem cells rather than BM microenvironments. Using the percentage of BP1+ B220+ pre-B cells in total BM lymphoid cells as a quantitative parameter, we studied the genetic control of BM pre-B cells in 159 F2 offspring of crosses between SL/Kh and NFS/N mice and 334 back-crosses to SL/Kh mice. A highly significant quantitative trait locus was identified on the distal segment of chromosome 3, showing logarithm of odds scores of 22.7 in the F2 cohort and 10.7 in back-cross mice. This quantitative trait locus, named bone marrow pre-B-1, colocalized with lymphoid enhancer factor-1, which encodes a high mobility group DNA-binding protein that is expressed in T and pre-B cells.

Animals↗
PubMed1999

Induction of tumor antigen-specific immunity in vivo by a novel vaccinia vector encoding safety-modified simian virus 40 T antigen.

BACKGROUND: Evidence that simian virus 40 (SV40) is associated with human mesotheliomas, osteosarcomas, and brain tumors suggests that a recombinant vaccine directed against lethal cancers expressing SV40 T antigen (Tag) could have clinical utility. To address this potential need, we designed a novel vaccinia virus construct that encodes an SV40 Tag in which oncogenic domains were excluded and immunogenic domains were preserved. We named this recombinant construct vaccinia-encoding safety-modified SV40 Tag (vac-mTag). METHODS: Purified vac-mTag was characterized by DNA sequencing, reverse transcription-coupled polymerase chain reaction, western blot analysis, and immunocytochemical techniques. Induction of Tag-specific immunity was examined by cytolytic T-cell assays, and the efficacy of vac-mTag in protecting animals against Tag-expressing tumors and in treating pre-established microscopic tumors was evaluated in vac-mTag-immunized BALB/c mice. RESULTS: The immune response elicited by vac-mTag in C57BL/6 and BALB/c mice included an SV40 Tag-specific cytolytic T-lymphocyte activity against syngeneic (identical genetic background) SV40 Tag-expressing tumor targets. Immunization of mice with a single dose of vac-mTag resulted in potent protection against subsequent challenge with a lethal mouse cancer expressing SV40 Tag. In addition, single-dose vac-mTag immunization coadministered with interleukin 2 produced a possible therapeutic effect against a preadministered microscopic (but lethal) burden of Tag-expressing tumor cells in vivo. CONCLUSION: vac-mTag induces an effective immune response in mice that is specific for a tumor-associated antigen. This response protects against a lethal tumor challenge and results in a possible therapeutic effect against Tag-expressing tumors in vivo. Thus, vac-mTag provides a new avenue for the development of therapies for human cancers thought to be associated with SV40.

Antineoplastic Agents↗
PubMed1999

Benign proliferative nipple duct lesions frequently contain CAM 5.2 and anti-cytokeratin 7 immunoreactive cells in the overlying epidermis.

Benign proliferative nipple duct lesions (PNDLs) pose a diagnostic problem for clinicians and pathologists. Clinically, they may be associated with skin changes typically present in Paget's disease of the nipple. The identification of numerous scattered cells in the epidermis that are immunoreactive for low-molecular-weight cytokeratin may lead to further confusion with Paget's disease. We studied the nipple epidermis in nine cases of PNDL and compared them with 26 histologically normal nipples from mastectomy specimens. CAM 5.2 and anticytokeratin 7 (CK7) immunoreactive cells were identified in the epidermis of seven of nine nipples associated with PNDL. The cytokeratin-positive cells appeared cytologically benign and were dispersed singly (scattered in seven of seven cases and frequent in four of seven cases) or formed small aggregates with occasional tubular structures (three of seven cases) in the basal and middle layers of the epidermis. In two of seven cases, these epidermal immunoreactive cells showed continuity with the underlying PNDL, suggesting the spread or continuation of lesional cells to the epidermis. Dispersed single immunoreactive cells were identified in small numbers (scattered) in the basal layer of the epidermis in 12 of 26 normal nipples and more frequently in 1 of 12 cases. In all cases, the intraepidermal cells were negative for carcinoembryonic antigen (CEA) and Her-2/neu. We conclude that intraepidermal CAM 5.2 and anti-CK7 immunoreactive cells, which are normally present in the nipple epidermis, may proliferate and form aggregates when there is an underlying PNDL. The presence of these cells does not imply Paget's disease when the intraepidermal cells have a bland cytologic appearance, fail to overexpress Her-2/neu, and there is no carcinoma within the PNDL or elsewhere in the breast.

Adult↗
PubMed1999

[Detection of K-ras mutations in colon cancer by PHA-PHFA (preferential homoduplex formation assay)].

The mutations of K-ras gene have been demonstrated at frequencies of about 40% in human colorectal cancer. We applied a developed PCR-preferential homoduplex formation assay (PCR-PHFA) to detect a point mutation of K-ras gene in the surgical specimens from thirty patients with colorectal cancer. This method is based on the strand competition during hybridization between a double labeled amplicon, prepared from biotin and DNP labeled primers, and an unlabeled amplicon. The procedure of this method is simple and speedy, and suitable to detect mutations in a small number of samples. By using this method, the mutations were found in 37% (11/30) and confirmed by sequencing analysis. The results suggest that the PCR-PHFA system may be useful for detecting low frequent mutation of K-ras gene even in the case of an early cancer.

Colorectal Neoplasms↗
PubMed1999

[Exploring into relationship between serum lipoprotein electrophoretogram and the differentiation as phlegm stasis syndrome of aged coronary heart disease patients].

OBJECTIVE: To observe the relationship between dynamic balance of the disturbance of serum lipoprotein and the 5 syndrome-types during Phlegm stasis syndrome (PSS) differentiation. METHODS: There were 171 patients, among them 81 cases were performed coronary arteriography (CAG). The serum lipoprotein electrophoretogram (SLPG) was examined by the double gradient polyacrylamide gel electrophoresis and the serum total cholesterol (TC) was determined with enzymatic method. RESULTS: (1) Comparing the PSS with the control group, there was significant difference in the abnormal items (P < 0.05-0.01). The blood stasis syndrome, PSS, and the Qi stagnation blood stasis syndrome were more than the phlegm syndrome and the non-PSS ones. The abnormal index of SLP (SLPI) had the following order: PSS(SLPI 1.941) > Qi stagnation blood stasis syndrome (1.901) > blood stasis syndrome (1.643) > phlegm syndrome (1.357) > non-PSS(1.105) and > the control syndrome (0.056). (2) The positive cases in CAG was 64 patients, in SLPG, it was 59 cases (92.19%). The negative in CAG was 17 cases, but the positive in SLPG, it was 14 cases (82.35%). (3) As the PSS developed further, the TC had an increasing tendency, but their average was less than 2100 mg/L, under the critical level. CONCLUSION: As the risk factor of the aged CHD, the TC was not an ideal criteria, the SPLG was an effective index. It was related with the PSS differentiation of the aged CHD.

Aged↗
PubMed1999

[Experimental study on ultrashort wave therapy on the healing of fracture].

The models of fracture in the rabbit radii were made. The rabbits in the experimental group were treated--with ultrashort wave at the fracture sites. The changes in the x-ray, histology, and biomechanics were observed dynamically. The results were that the speed and quality of the fracture healing in the experimental group were much better than in the control group.

Animals↗
PubMed1999

[Clinical analysis of percutaneous balloon mitral valvotomy in 1063 patients].

This article reports the clinical study of 1063 patients who underwent percutaneous balloon mitral valvotomy (PBMV) and 1043 patients among them who did successfully (98.2%). After the procedure, left atrial mena pressure fell from 3.19 +/- 1.06 kPa to 2.00 +/- 0.93 kPa (P < 0.001), mitral pressure gradient decreased from 2.79 +/- 1.20 kPa to 1.33 +/- 1.06 kPa (P < 0.001). Disappearance of diastolic murmur and significant improvement of cardiac function were achieved. Among the 20 failed cases, there were cardiac perforation and/or pericardial tamponade (8 cases), cerebral embolism (3 cases), severe mitral regurgitation (3 cases), atrial septal defect (2 cases) and discontinuance of the procedure due to various causes. The short-term outcome of PBMV is satisfying, so it can replace the surgical closed valvotomy as an effective treatment for selected patients with mitral stenosis.

Adolescent↗
PubMed1999

[Study on the mechanism of glutamate mediated neurotoxicity by cortical neuron culture technique in vitro].

This study was intended to further explain the mechanism of glutamate (Glu) mediated neurotoxicity. The concentrations of TCa and Ca2+ i were measured in 32 cortical neuron cultures, which were divided into four groups: normal control group (n = 8); 0.5 mmol/L Glu group (Glu group n = 8); 0.5 mmol/L Glu + 100 mmol/L Nimodipine group (antagonist I, n = 8); 0.5 mmol/L Glu + 12 mumol/L MK-801 group (antagonist II, n = 8). The results showed that TCa and Ca2+ i concentrations in Glu group were significantly higher than those in normal control group (P < 0.05); TCa and Ca2+i in both antagonist I and II groups were evidently lower than those in Glu group (P < 0.05); No difference was found between antagonist I and II groups. The results suggest that Glu neurotoxicity is due to the intracellular calcium overload, which may be from the pathway of voltage-dependent calcium channels (VDCCs) and NMDA receptor-operated channels (NROCs).

Animals↗
PubMed1999

Characterization of eprinomectin N-deacetylase in rats.

The enzyme system responsible for the N-deacetylation of eprinomectin in rats was characterized. Tissue and subcellular studies showed that the hydrolysis activity was localized mainly in liver microsomes. Apparent KM and Vmax values calculated from Lineweaver-Burk plots were 53 microM and 0.81 nmol/mg/min for male rats and 70 microM and 4.99 nmol/mg/min for female rats, respectively. Pretreatment of male rats with dexamethasone, phenobarbital, and pregnenolone 16alpha-carbonitrile increased the activity by more than 3-fold. Paraoxon and bis-4-nitrophenylphosphate strongly inhibited the deacetylase activity at concentrations as low as 1 microM. The hydrolysis activity also was inhibited by SKF525, but less effectively. Eserine strongly inhibited the activity at 1 x 10(-4) M. HgCl2 decreased the activity to about 40% at a concentration of 1 x 10(-4) M. FeCl3, CaCl2, MgCl2, and EDTA had little effect on the hydrolysis of eprinomectin, whereas NaF slightly increased the activity to 118%. Thus, the inhibition study suggested that eprinomectin deacetylase resembled "B" type carboxylesterase/amidases. The hydrolysis activity of eprinomectin and isocarboxazid, a specific substrate of RL2 [Hosokawa, M, Maki T and Satoh T (1987) Mol Pharmacol 31:579-584], by liver microsomes from rats treated with various cytochrome P-450 inducers correlated well (r = 0.92). Also, elusion profiles of esterase by gel filtration and ion exchange chromatography demonstrated that the active protein(s) for eprinomectin and isocarboxazid hydrolysis coeluted. Thus, RL2 or an enzyme system similar to RL2 is responsible for the N-deacetylation of eprinomectin.

Amidohydrolases↗
PubMed1998

[Establishment of partial gene expression map of 7q32 in nasopharyngeal carcinoma and primary culture normal nasopharyngeal epithelial cells].

OBJECTIVE: To establish partial gene expression map of 7q32 in nasopharyngeal carcinoma (NPC) cell line, tissues and primary culture normal nasopharyngeal epithelial cells. METHODS: We detected the expression of 20 ESTs at 7q32 in NPC cell line HNE1,13 NPC biopsies and primary culture normal nasopharyngeal epithelial cells using differential RT PCR and Northern hybridization. RESULTS: 8 ESTs (AA188181, AA13079,N27556, AA031919, N22721, H20825, T91284, AA001936) expressed equally in both of HNE1 and primary culture normal nasopharyngeal epithelial cells; 7 ESTs (T64215, AA025822, R60014,R80002,H06688, R60192,R95096) expressed in neither of them; 3 ESTs (H19830,W72688,AA130630) overexpressed in HNE1 ; and 2 ESTs (AA070437, H90882) overexpressed in primary culture normal nasopharyngeal epithelial cells. W72688 and H19830 each overexpressed in 77%(10/13) of NPC biopsies; AA070437 down-expressed in 30.7% of NPC biopsies. CONCLUSION: Partial gene expression map of 7q32 in nasopharyngeal carcinoma cell line ,tissues and primary culture normal nasopharyngeal epithelial cells has been established. The up-regulation of W72688, H19830 and down-regulation of AA070437 may be related to the occurrence of NPC.

Blotting, Northern↗
PubMed1998

No heroin or morphine 6beta-glucuronide analgesia in mu-opioid receptor knockout mice.

Recent reports suggest that heroin and its metabolite morphine 6beta-glucuronide can produce analgesia independent of the morphine-preferring mu-opioid receptor. We have tested heroin and morphine 6beta-glucuronide analgesia in wild-type, homozygous and heterozygous mu-opioid receptor knockout mice. Homozygotes display no heroin or morphine 6beta-glucuronide analgesia. Heterozygous mice with one mu-opioid receptor gene copy reveal reduced heroin and morphine 6beta-glucuronide analgesia. The mu-opioid receptor-dependence of heroin and morphine 6beta-glucuronide fails to support a requirement for a heroin-specific opiate receptor subtype.

Analgesia↗
PubMed1998

Cocaine reward models: conditioned place preference can be established in dopamine- and in serotonin-transporter knockout mice.

Cocaine and methylphenidate block uptake by neuronal plasma membrane transporters for dopamine, serotonin, and norepinephrine. Cocaine also blocks voltage-gated sodium channels, a property not shared by methylphenidate. Several lines of evidence have suggested that cocaine blockade of the dopamine transporter (DAT), perhaps with additional contributions from serotonin transporter (5-HTT) recognition, was key to its rewarding actions. We now report that knockout mice without DAT and mice without 5-HTT establish cocaine-conditioned place preferences. Each strain displays cocaine-conditioned place preference in this major mouse model for assessing drug reward, while methylphenidate-conditioned place preference is also maintained in DAT knockout mice. These results have substantial implications for understanding cocaine actions and for strategies to produce anticocaine medications.

Animals↗
PubMed1998

Cloning and characterization of a novel human chemokine receptor.

The present study reports the identification of a human gene, HCR, which encodes a novel human chemokine receptor. The partial sequence of the HCR gene was first found in a human neutrophil cDNA library. With the use of an expressed sequence tag (EST) probe from the neutrophil library, the full length HCR cDNA was isolated. The open reading frame of HCR cDNA predicts a protein of 345 amino acids with seven transmembrane domain topography. The HCR gene exhibits good homology to human MIP-1a receptor with 43.1% amino acid identity and 64.4% amino acid similarity and also shows considerable sequence homology to other human chemokine receptors such as the MCP-3 receptor, MCP-5 receptor, and MCP-1 receptor. Northern blot analysis suggests that HCR gene is expressed abundantly in immunal tissues such as spleen, fetal liver, lymph node, and bone marrow. Strong expression was also found in human lung and heart. A chromosome mapping study indicated that HCR gene is positioned within human chromosome band Xq13. Our result suggests that HCR gene is a novel putative chemokine receptor.

Amino Acid Sequence↗
PubMed1998

Cloning of a putative human neurotransmitter receptor expressed in skeletal muscle and brain.

With the use of the degenerated nucleotides that contain the conserved sequence of G protein-coupled receptor, we have identified a 648-bp clone (HDGRC02) from human genomic DNA with significant sequence homology to human neurotransmitter receptors. HDGRC02 was then used as a probe for the screening of full length gene. From human Lambda DASH II genomic library, a 1.6 Kb clone encoded a full length gene was isolated and named putative neurotransmitter receptor (PNR). PNR has a single open reading frame which predicts a 38.3 KD protein of 338 amino acids with seven transmembrane domain topography. The amino acid sequence of PNR exhibits considerable homology to the rat 5-HR1D receptor with 35% amino acid identity and 56% amino acid similarity. PNR also shows significant sequence homology to the 5-HT1D receptor from Japanese puffer fish fugu, to the 5-HT4L receptor from mouse, to the alpha-2 adrenergic receptor and to the D2 dopamine receptor. Northern blot analysis indicates that PNR is expressed in skeletal muscle and selected areas of the brain. A chromosome mapping study located the PNR gene with human chromosome band of 6q23. The findings in the present study demonstrate that PNR is a putative neurotransmitter receptor.

Amino Acid Sequence↗
PubMed1998

Identification of cytochrome P4503A4 as the major enzyme responsible for the metabolism of ivermectin by human liver microsomes.

1. Ivermectin was extensively metabolized by human liver microsomes to at least 10 metabolites. The structure of many of them (mostly hydroxylated and demethylated) was determined by 1H-NMR and LC/MS. 2. To determine which human cytochrome P450 isoform(s) is responsible for the metabolism of ivermectin, chemical inhibitors including sulphaphenazole, quinidine, furafylline, troleandomycin (TAO) and diethyldithiocarbamate (DDC) were used to evaluate their effect on ivermectin metabolism. TAO, a specific inhibitor of cytochrome P4503A4, was the most potent inhibitor, inhibiting the total metabolism as well as formation of each metabolite. Metabolism was also inhibited by an anti-human cytochrome 3A4 antibody by 90%. 3. When ivermectin was incubated with microsomes from cells expressing CYP1A1, 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 or 3A4 at 4 mg/ml protein concentrations, metabolic activity was only detected with the microsomes containing CYP3A4. The metabolic profile from cDNA-expressed CYP3A4 microsomes was qualitatively similar to that from human liver microsomes. 4. Thus, cytochrome P4503A4 is the predominant isoform responsible for the metabolism of ivermectin by human liver microsomes.

Chromatography, High Pressure Liquid↗
PubMed1998

Cloning, characterization, and mapping of human homolog of mouse T-cell death-associated gene.

To establish immunologic autotolerance, self-reactive immature thymocytes are eliminated by negative selection during T-cell development in the thymus. Self-reactive clones undergo apoptosis after stimulation via the T-cell receptor (TCR). The process of cell selection is determined by the dedication of the TCR for tolerogenic antigen/major histocompatibility complex. We have cloned a novel human gene that is highly homologous in the transmembrane and G protein-coupling domains to mouse T-cell death-associated gene 8 (TDAG8). The gene, human TDAG8 (hTDAG8), which belongs to the G protein-couple receptor superfamily, encodes a protein of 337 amino acids. An expressed sequence tag (EST) corresponding to hTDAG8 was identified from a human thyroid cDNA library and subsequently used to isolate a full-length genomic clone. Northern blot analysis revealed that the hTDAG8 gene is expressed predominantly in lymphoid tissues, including peripheral blood leukocytes, spleen, lymph nodes, and thymus. Stably transfected mammalian CHO cells were generated, and heterologous expression of hTDAG8 was confirmed by Northern blot analysis. Fluorescent in situ hybridization (FISH) revealed that hTDAG8 maps to human chromosome 14q31-32.1, a region in which abnormalities associated with human T-cell lymphoma or leukemia are found. Taken together, these data implicate the hTDAG8 gene in T-cell-associated diseases in humans, but its actual physiological and pathological role in the human immune system needs further investigation.

Amino Acid Sequence↗
PubMed1998

Immunoreactive endothelin-1 and its receptors in human adrenal tissues.

To elucidate the pathophysiologic significance of endothelin-1 (ET-1) in adrenal and the mechanism for reduced responsiveness to exogenous ET-1 in aldosterone-producing adenoma (APA), we have investigated ET-1 receptors by radioligand binding assay (RBA) in human normal adrenal (NA), APA, idiopathic hyperaldosteronism (IHA), and pheochromocytoma (PHEO), immunoreactive (ir-) ET-1 content in NA, APA and PHEO by radioimmunoassay (RIA), and immunohistochemical staining of ET-1 with the peroxidase-anti-peroxidase (PAP) method in NA, APA, and PHEO. A single class of high-affinity binding sites for ET-1 was found in human NA and tumor tissues. Dissociation constant (Kd) values of ET-1 receptors were similar in NA, APA, and IHA, but maximal binding capacity (Bmax) of ET-1 receptors was lower in APA than in NA and IHA. Both Kd and Bmax in PHEO were higher than those in NA, APA, and IHA. Ir-ET-1 content in tumors of APA and PHEO were higher than in NA. Immunohistochemical staining was more intense in the tumor cells of APA and PHEO than in NA. These results suggest that the reduced response to exogenous ET-1 in APA could be related to downregulation of ET-1 receptors in the tumor. Increased ET-1 content and receptors may lead to hypersecretion of catecholamine in PHEO. ET-1 produced in normal and tumor adrenal tissues may regulate aldosterone and catecholamine secretion from adrenals in a paracrine/autocrine fashion.

Adrenal Gland Neoplasms↗